192 Mediastinitis
Acute Anterior Mediastinitis
Rarely, acute anterior mediastinitis may occur without antecedent median sternotomy, as reported after traumatic sternal fracture1 or as a consequence of descending cervical infections (see later), but by far the most common form of acute mediastinitis is that occurring after sternotomy for a cardiac operation. The term mediastinitis after cardiac operations should strictly refer to an infection involving the space behind, deep to, the sternum. Post–cardiac surgery infections may more broadly include those that are superficial or subcutaneous “above” the fascia, unassociated with sternal pathology, and those that involve the sternum itself (sternal osteomyelitis or sternitis) without deeper infection. For purposes of the following discussion, we will assume any infection posterior to the sternum is an infection of the anterior mediastinum, including those patients with deep sternal infections, as no impervious anatomic barrier exists between the posterior cortex of the sternum and the space behind it. Deep sternal infection can be considered one end of the spectrum of mediastinitis, with the other being gross pus in the anterior mediastinum and pericardium (deep organ space infection). There are, of course, patients who have sterile sternal dehiscence with no evidence of infection, but this is a diagnosis of exclusion, so that these patients are treated with antibiotics and/or irrigation pending culture results. In patients who have sterile postoperative sternal wound drainage, there is a real opportunity for retrograde infection. Clinically, especially in more obese patients, it is sometimes unclear as to whether one is initially dealing with a superficial problem (anterior to the fascia), a sterile dehiscence, or a deeper infection. More than a small amount of drainage, any sternal instability or evidence of separation (e.g., broken wires on a chest film) suggest at least a sterile dehiscence and the need for reexploration, deep cultures, and appropriate re-closure.
Incidence, Pathology and Prevention
Even among large well-reported series, the incidence of post–cardiac surgery mediastinitis varies, as noted earlier, due in part to the various definitions of mediastinitis, sternal osteomyelitis, or deep sternal wound infection. On occasion, the diagnosis may be made weeks or months after hospital discharge, and that occurrence may be missed by the institution where the operation was originally performed. Over the past 2 decades, there may be a trend toward lower reported rates of mediastinitis after sternotomy (more large series with <1% incidence), but the reported range remains wide, from 0.24% to 4% of cardiac operations.2,3,4 Increasingly, as the postoperative length of stay decreases, mediastinal infections are diagnosed days or even months after hospital discharge, with median time to diagnosis variously reported around 10 days after the index cardiac operation.
In October 2008 the Centers for Medicare and Medicaid declared post–cardiac surgery mediastinitis a “preventable condition,”5 but no existing data manifest it as entirely preventable. Indeed, a number of mostly unmodifiable host factors that increase the risk of post–cardiac surgery mediastinitis have been identified. Among these are diabetes, increased body mass index, older age, renal failure, prolonged preoperative hospitalization, immunosuppression, chronic obstructive pulmonary disease, cigarette smoking, reoperation, preoperative atrial fibrillation, and elevated C-reactive protein.3,6,7
In addition to host factors, intraoperative factors influence the risk. An increased incidence of deep sternal wound infection has been associated with bilateral internal mammary use, prolonged operative time, and use of the intraaortic balloon pump.7 Postoperative management may also influence the risk of mediastinitis; increased glucose levels (>200 mg/dL),8 reexploration, and prolonged ventilator use are associated with a higher incidence of deep sternal infection.7 Glucose values as low as ≥130 mg/dL have been linked to such infection in children.9 Undoubtedly factors such as skin preparation, electrocautery use, glove changes, and attention to a host of other details account for some of the variation in infection rates from surgeon to surgeon and institution to institution. Avoiding sternotomy entirely, as can be done with less chest wall–invasive approaches, appears to drastically reduce or eliminate the risk of mediastinal infection after cardiac operations.7
Postoperative tracheostomy is required in some post-sternotomy patients, and many of these have some of the risk factors that are also predictive of deep sternal wound infection. Open tracheostomy for patients with prolonged ventilator dependence, once deferred 2 or more weeks after sternotomy for fear of contaminating the anterior mediastinal space, has not been shown to be associated with an increased incidence of mediastinitis (mean of 5.6 days post cardiac operation).10 Specifically, the technique of percutaneous tracheostomy has not been associated with subsequent mediastinal infection. This technique may allow an earlier, safer switch from an oral to cervical airway11 in patients requiring prolonged mechanical ventilation.
Staphylococcal species are the most common organisms seen in patients with post-sternotomy deep wound infection, and these are increasingly methicillin resistant.12 Coagulase-negative resistant organisms are more common in patients who have prolonged hospitalizations.13 Gram-negative organisms may be cultured, particularly from diabetics, in patients with gram-negative pneumonia prior to operation, or in those who require reexploration.14
The serious consequences of mediastinitis after cardiac operations dictate the use of prophylactic antibiotics as an established practice. Given the most common organisms causing these infections, a second-generation cephalosporin is still the most accepted prophylaxis. A commonly used regimen would include cephazolin, 2 g, within 1 hour of skin incision, with a second 1-g dose at 3 to 4 hours if the incision remains open. Vancomycin is substituted in patients with penicillin allergy, in deference to the possibility of cross-reactivity, and it may be used routinely for an interval in institutions experiencing an outbreak of resistant staphylococci. The addition of preoperative gram-negative coverage (e.g., gentamicin) is appropriate in such cases, given vancomycin’s poor coverage of such organisms.15 Topical vancomycin has been shown effective in decreasing the incidence of sternal infections, and although used routinely in some practices, the development of resistant staphylococci is a genuine concern.16 An evidence-based guideline from the Society of Thoracic Surgeons recommends gram-positive prophylaxis for no more than 48 hours, in addition to preoperative nasal mupirocin.12,15
Diagnosis
The gravity of the diagnosis and variability of clinical signs has encouraged the use of imaging techniques to confirm or refute the possibility of deep sternal or mediastinal infection. Unfortunately, the variable diagnostic accuracy of most of these techniques permits them to be supportive17 but rarely if ever definitive in the diagnosis of deep infection. This is especially true in the early time frame (<30 days) when the vast majority of patients present. During this time, fluid collections and mediastinal soft-tissue changes are common, if not universal, both being nonspecific for infection.18 Nuclear studies (99mTc) have been used in late-presenting indolent cases in an attempt to separate sternal involvement from infections superficial to it.19 All these imaging studies are, of course, confounded by changes that one can expect following the operative procedure itself. A profile of abnormal cytokine levels has been characterized,20 with terminal SC5b-9 complement complex concentration being substantially higher in patients with mediastinitis, and having no overlap with values in non-mediastinitis, post–cardiac surgery controls. In difficult to diagnose cases, blind retrosternal, subxiphoid needle aspiration and culture has been variably employed, and aspiration with ultrasound guidance has been reported after cardiac transplantation.21 A recent small series suggested diagnostic success in patients without classic signs of infection by anteriorly inserting a 22-gauge needle percutaneously and aspirating between the recently closed sternal edges. Cultures and Gram stains were used to establish the presence of infection, with a high degree of specificity and sensitivity.22
Treatment
While the need for operative treatment in anterior mediastinitis is firmly established, the techniques successfully employed vary greatly. The varied technical approaches are related to the timing of diagnosis (interval since antecedent operation), the depth-extent of infection, and the acuity of the patient. The experience and choice of the treating surgeon is also a factor in the technique used to manage a deep infection. In patients with suspected infection in whom there is drainage and some sternal instability, expeditious reexploration with débridement of the sternal edges and surrounding soft tissues, accompanied by irrigation and drainage may permit sternal re-wiring.2,23 In patients who are septic, and/or in those with gross retrosternal purulence, a staged approach or immediate tissue coverage may be employed.
If sternal re-closure is elected after débridement an alternative wiring technique, either a variation of the Robicsek24 weave or a commercially available plate fixation device, is generally used. Cultures obtained at operation dictate the systemic antibiotics ultimately used, but initial coverage may include a second-generation cephalosporin and gram negative coverage until gram stain or culture results are definitive. A variety of irrigation solutions and protocols have been employed in these patients. Diluted antibiotic, povidone iodine, and aqueous acid solutions have been reported.23,25 The duration of irrigation has varied from three days to a week, while systemic antibiotics are continued, as would be the case for other adult bone infections. Unfortunately, this attempt at primary sternal closure has been reported to require secondary procedures in 20% to 40% of the patients.26 More recently, one small series23 employing the single-stage débridement, closure, and irrigation technique had success in 95% of patients so treated.
A two-stage approach involves an interval during which the sternum and skin are left open and a wound vacuum device placed.27,28 Open management of sternal wounds is associated with a risk of sudden, sometimes fatal, cardiac hemorrhage from exposed grafts, the aorta, or (most frequently) the right ventricle. Needless to say, the risk of death in such patients is very high (>50%).29,30,31 Given these risks, it has been recommended that close attention be paid to the proximity of the right sternal edge and the right ventricle or grafts. Decreased abrasive contact may be afforded by judicious use of sedation and mechanical ventilation until coverage can be achieved.
Whether used as an initial single-stage procedure or as a secondary procedure, tissue transposition into the anterior mediastinum has dramatically changed the prognosis of this once often fatal complication.32 Well-vascularized omentum or muscle can be used. Muscle options include rollover of the pectoralis major (detached from its humeral insertion, leaving intact the muscle’s origin and blood supply) or rotation and advancement of the pectoralis major (detached from its costal origins and thereby maintaining its lateral blood supply). The rectus abdominis muscle may, depending on the prior use of the ipsilateral mammary artery, be detached distally and rotated on its cephalad attachment into the anterior mediastinal space. The omentum may be based on the right gastroepiploic or mobilized, leaving the gastroepiploic intact. The sternum may be left open with the tissue flap between the remnant edges, or rarely it may be closed over the flap. Either way, closed suction drains are required for the large, mobilized skin flaps and sometimes beneath transposed tissue flap.
The use of omentum versus any specific muscle flap may be dictated by availability (e.g., in patients with prior laparotomies), but when the option exists, the use of omentum has been touted as advantageous over muscle flaps,33 although it has also been cited as being associated with poorer survival outcome,34 perhaps related to patient selection. It has also been successfully employed in infections after ascending aortic replacement.35 Skin coverage over a transposed flap may be accomplished by primary presternal skin reapproximation, split-thickness skin grafting, or, with the rectus muscle, a skin paddle may be transposed as well.
As noted earlier, débrided sternal wounds may be prepared for flap coverage by the use of a closed high-pressure vacuum system in which a polyurethane foam (400-600 µm pore size) is cut to fit the anterior mediastinal space and sealed to the skin permitting a vacuum (negative 75 mm Hg) to be generated over the entire wound surface. The device is changed regularly to avoid tissue ingrowth. Particularly with smaller wounds, the vacuum treatment may obviate the use of flap coverage as the wound heals secondarily, with obliteration of the space over a period of weeks.36,37
Prognosis
Although the mortality of mediastinitis has improved dramatically over the past 2.5 decades, the likelihood of death remains high. Early detection with expeditious operative débridement and tissue coverage are the major advances that have allowed that improvement to take place. Still, the acute in-hospital mortality with post-sternotomy mediastinitis reported in larger series has ranged from 12.8% to 47%.2,38 Patients may die of sepsis or hemorrhage, either as a consequence of direct cardiac injury or secondary to an infected graft or foreign body. More often, death occurs from associated comorbidities or complications, especially an additional infection,38 that accompany the mediastinal infection. An examination of the predictors for deep sternal infection illuminates the fact that patients who develop this serious complication are more likely to have multiple comorbidities that might limit their survival. Importantly, it is not merely the acute mortality that is elevated in patients with post–cardiac surgery mediastinitis. In studies from the Northern New England Cardiovascular Disease Study Group, adjusting for various comorbidities, the 4-year mortality for patients with a postoperative deep sternal infection was 3 times greater than those without that complication, and this increased all-cause mortality rate persisted with up to 10 years of follow-up. For patients surviving more than 6 months after cardiac operation, the incidence of death was 70% higher than the rate among patients who did not have mediastinal infection.39
Posterior Mediastinitis
Acute infections that arise in the posterior mediastinum generally result from disease that may be primary to the esophagus or, more commonly in the United States, secondary to some esophageal intervention. Primarily, esophagitis (e.g., in immunocompromised patients with fungal or viral organisms) may extend through the esophagus, resulting in mediastinitis. Abscess formation, presumably secondary to hematogenous spread, has been reported40 in a dialysis patient. More commonly, infection of the posterior mediastinum is the result of esophageal instrumentation (scopes, probes, tubes, or dilators), and even esophageal ultrasound-guided needle biopsy may result in abscess.41 Esophageal perforation (often at the gastric junction) from a swallowed foreign body (e.g., bone or toothpick) has been reported.42 Esophageal operations may be the source of an infection due to anastomotic disruption, but as transhiatal esophagectomy is increasingly employed for patients with esophageal cancer, its cervical gastropharyngeal anastomosis mostly avoids the consequences of mediastinitis. Still, among patients having an intrathoracic esophagogastric anastomosis, a leak may occur in 4.3% to 8.7% of patients.43 Traumatic injuries to the trachea, proximal bronchii, or esophagus obviously may result in contamination of this space as well. Other causes of posterior compartment mediastinitis include the classic Boerhaave’s syndrome characterized by rupture of the lower esophagus post retching and, more rarely, the erosion of a broncholith from a partially or completely obstructed bronchus.44
Diagnosis
Suspicion of posterior mediastinitis should be heightened by any of the mentioned historical factors, and additionally may include prior symptoms of dysphagia. Given a relevant history, the presence of cervical pain and/or chest pain with a high fever would strongly suggest the diagnosis. On examination, supraclavicular crepitus may be identified in patients with upper mediastinal pathology but would generally be absent initially in those with middle or lower esophageal disease. Leukocytosis might be a singular early laboratory abnormality. Depending on the underlying pathology and duration of contamination, sepsis with mental status changes and hypotension may occur. Certainly in some of these patients, the plain chest film reveals a pleural effusion, and more rarely, air may be seen in the retropharyngeal space or other abnormal locations along the length of the mediastinum posterior to the pericardium. Computed tomography (CT) scan with oral Gastrografin is the mainstay for diagnosis and localization, as it can clearly demonstrate any abnormal air or fluid collections along the esophagus or esophagogastric junction, and water-soluble contrast might diagnose the presence of an esophageal leak. A more indolent subacute presentation might be accompanied by a distinct fluid collection or abscess in the mediastinum. Transesophageal ultrasonography and fine-needle aspiration have been jointly used to diagnose a variety of periesophageal infections,45 and this bedside technique in critically ill patients likely has improved diagnostic accuracy over standard CT imaging.
Treatment
Clearly, some low-grade mediastinitis must occur with any transmural disruption of the esophagus. Stable patients thought likely to have a recent disruption (hours) can have a dilute barium swallow. A contained esophageal disruption (usually the result of instrumentation) is manifest by extravasation of contrast that drains rather promptly back into the lumen. Such injuries may be managed successfully by serial clinical evaluation, limited oral intake, antibiotic therapy, and repeat imaging.46 This may be particularly true in young children.47 In patients with more frank mediastinal contamination not confined to the local perforation but identified within the first 24 hours, operation with primary repair and drainage is most often indicated.48,49 If the time since perforation is sufficiently short and the injury sufficiently small, so that local inflammation is limited, primary repair of a disruption—preferably with viable vascularized tissue buttressing—has been successfully employed,49 even after 24 hours.50 Success has also been recently reported using covered self-expanding esophageal stents.51 Image-guided nonoperative drainage with antibiotics has been successfully employed in selected cases where a defined collection or abscess can be identified.
In patients with more extensive local inflammation, those diagnosed more than 24 hours after perforation, and those who are more systemically ill, drainage with or without some esophageal diversion may be employed. A variety of procedures for upper alimentary tract diversion have been described, from simple nasogastric suction to cervical esophagostomy with gastrostomy. If the diagnosis of posterior mediastinal infection is made sufficiently early, prior to the development of sepsis, adequate local drainage and antibiotic therapy are adequate therapy. In such situations, some have advocated resection of the involved esophagus with appropriate diversion and drainage. Alimentary continuity can then be restored after recovery from the mediastinal infection.48 Continued sepsis and multiple organ failure are the most common cause of death among these patients, and multiple operations to excise necrotic tissue and drain the space are sometimes required before definitive reconstruction.
Migratory and Chronic Mediastinal Inflammation
The mediastinum may be infected secondarily from contiguous acute infections involving adjacent anatomic spaces. Pleural or pulmonary processes may transgress the mediastinal envelope, as may infections of the spine, particularly the vertebral bodies. Mediastinitis has been reported secondary to intraabdominal processes from subdiaphragmatic abscesses52 to retroperitoneal extension of colonic infections. Perhaps the most dramatic and well described of the migratory mediastinal infections are those that descend from the neck and known as descending necrosing mediastinitis. These include those infections that arise as classic Ludwig’s angina (odontogenic or nonodontogenic) or from cervical puncture wounds. Gravity and the negative pressure of the thoracic cavity have been cited as reasons for this descent through the pretracheal space into the upper posterior mediastinum. The patients are often young and may have a history of a dental infection. Cervical pain, cellulitis, necrosis, and abscess formation may occur, and a high index of suspicion leading to CT imaging can be diagnostic. Broad-spectrum antibiotics are essential and must be accompanied by cervical and mediastinal drainage directed by the clinical and radiologic findings.53,54 Drainage may be accomplished in a variety of ways including right thoracotomy, left-sided video-assisted thoracoscopy, or an anterior clamshell incision. The mortality of this condition has historically ranged from 20% to 40% and increases directly with the interval between onset of symptoms and diagnosis. Oropharyngeal cervical infections descending into the mediastinum have been successfully managed with antibiotics and a combination of percutaneous drains and/or videoscopic débridement.52,55 In any case, aggressive imaging surveillance and a commitment to achieving and maintaining adequate drainage (multiple varied procedures) are necessary to successful management of this relatively rare life-threatening disorder.56
Mediastinal fibrosis is a chronic condition that may present precipitously when the process constricts a mediastinal structure compromising its lumen. Pulmonary vein, pulmonary artery,57 vena caval,58 and tracheal stenoses have been seen most commonly. The diagnosis is generally established by CT or magnetic resonance imaging (MRI) which reveals a diffusely infiltrating, sometimes calcified, mass. Bronchoscopy may contribute to the diagnosis.59 The fibrosis is a benign, acellular proliferation of fibrous collagenous tissue which is idiopathic or may be an immunologic sequela of an intervention (e.g., radiofrequency ablation) or infection (mycotic, specifically and most commonly Histoplasma).60,61 Treatment may include steroid therapy62 and local dilation of stenotic lumina with stents or operation.63
Prevention of Post–Cardiac Operation Mediastinitis:
Edwards FH, Engelman RM, Houck P, Shahian DM, Bridges CR. The Society of Thoracic Surgeons practice guideline series: antibiotic prophylaxis in cardiac surgery, part I: duration. Ann Thorac Surg. 2006;81:397-404.
Engelman RM, Shahian DM, Shemin R, Guy TS, Bratzler D, Edwards F, et al. The Society of Thoracic Surgeons practice guideline series: antibiotic prophylaxis in cardiac surgery, part II: antibiotic choice. Ann Thorac Surg. 2007;83:1569-1576.
Management of Post–Cardiac Operation Mediastinitis:
Ennker IC, Pietrowski D, Vohringer L, Kojcici B, Albert A, Vogt PM, et al. Surgical debridement, vacuum therapy and pectoralis plasty in poststernotomy mediastinitis. J Plast Reconstr Aesthet Surg. 2009;62:1479-1483.
Management of Esophageal Perforation:
Abbas G, Schuchert MJ, Pettiford BL, Pennathur A, Landreneau J, Landreneau J, et al. Contemporaneous management of esophageal perforation. Surgery. 2009;146:749-755.
Blackmon SH, Santora R, Schwarz P, Barroso A, Dunkin BJ. Utility of removable esophageal covered self-expanding metal stents for leak and fistula management. Ann Thorac Surg. 2010;89:931-937.
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6 Gummert JF, Barten MJ, Hans C, Kluge M, Doll N, Walther T, et al. Mediastinitis and cardiac surgery–an updated risk factor analysis in 10,373 consecutive adult patients. Thorac Cardiovasc Surg. 2002 Apr;50(2):87-91.
7 Elenbaas TW, Soliman Hamad MA, Schonberger JP, Martens EJ, van Zundert AA. Preoperative atrial fibrillation and elevated C-reactive protein levels as predictors of mediastinitis after coronary artery bypass grafting. Ann Thorac Surg. 2010 Mar;89(3):704-709.
8 Zerr KJ, Furnary AP, Grunkemeier GL, Bookin S, Kanhere V, Starr A. Glucose Control Lowers the Risk of Wound Infection in Diabetics After Open Heart Operations. Ann Thorac Surg. 1997;63:356-361.
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10 Gaudino M, Losasso G, Anselmi A, Zamparelli R, Schiavello R, Possati G. Is early tracheostomy a risk factor for mediastinitis after median sternotomy? J Cardiac Surg. 2009 Nov-Dec;24(6):632-636.
11 Hubner N, Rees W, Seufert K, Bockelmann M, Christmann U, Warnecke H. Percutaneous dilatational tracheostomy done early after cardiac surgery–outcome and incidence of mediastinitis. Thorac Cardiovasc Surg. 1998 Apr;46(2):89-92.
12 Edwards FH, Engelman RM, Houck P, Shahian DM, Bridges CR. The Society of Thoracic Surgeons Practice Guideline Series: Antibiotic Prophylaxis in Cardiac Surgery, Part I: Duration. Ann Thorac Surg. 2006 Jan;81(1):397-404.
13 Tegnell A, Aren C, Ohman L. Coagulase-negative staphylococci and sternal infections after cardiac operation. Ann Thorac Surg. 2000 Apr;69(4):1104-1109.
14 Gardlund B, Bitkover CY, Vaage J. Postoperative mediastinitis in cardiac surgery – microbiology and pathogenesis. Eur J Cardiothorac Surg. 2002 May;21(5):825-830.
15 Engelman RM, Shahian DM, Shemin R, Guy TS, Bratzler D, Edwards F, et al. The Society of Thoracic Surgeons Practice Guideline Series: Antibiotic Prophylaxis in Cardiac Surgery, Part II: Antibiotic choice. Ann Thorac Surg. 2007;83:1569-1576.
16 El Oakley R, Nimer KA, Bukhari E. Is the use of topical vancomycin to prevent mediastinitis after cardiac surgery justified? J Thorac Cardiovasc Surg. 2000 Jan;119(1):190-191.
17 Misawa Y, Fuse K, Hasegawa T. Infectious mediastinitis after cardiac operations: computed tomographic findings. Ann Thorac Surg. 1998 Mar;65(3):622-624.
18 Yamaguchi H, Yamauchi H, Yamada T, Ariyoshi T, Aikawa H, Kato Y. Diagnostic validity of computed tomography for mediastinitis after cardiac surgery. Ann Thorac Cardiovasc Surg. 2001 Apr;7(2):94-98.
19 Quirce R, Carril JM, Gutierrez-Mendiguchia C, Serrano J, Rabasa JM, Bernal JM. Assessment of the diagnostic capacity of planar scintigraphy and SPECT with 99mTc-HMPAO-labelled leukocytes in superficial and deep sternal infections after median sternotomy. Nucl Med Commun. 2002 May;23(5):453-459.
20 Risnes I, Ueland T, Aukrust P, Lundblad R, Baksaas ST, Mollnes TE, et al. Complement activation and cytokine and chemokines release during mediastinitis. Ann Thorac Surg. 2003 Mar;75(3):981-985.
21 Bernabeu-Wittel M, Cisneros JM, Rodriguez-Hernandez MJ, Martinez A, Ordonez A, Martinz M. Suppurative mediastinitis after heart transplantation: early diagnosis with CT-guided needle aspiration. J Heart Lung Transplant. 2000 May;19(5):512-514.
22 Benlolo S, Matéo J, Raskine L, Tibourtine O, Bel A, Payen D, Mebazaa A. Sternal puncture allows an early diagnosis of poststernotomy mediastinitis. J Thorac Cardiovasc Surg. Mar 2003;125:611-661.
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24 Robicsek F, Daugherty HK, Cook JW. The prevention and treatment of sternum separation following open-heart surgery. J Thorac Cardiovasc Surg. 1977;73:267-268.
25 Hayashi H, Kumon K, Yahagi N, Haruna M, Watanabe Y, Matsui J, et al. Successful treatment of mediastinitis after cardiovascular surgery using electrolyzed strong acid aqueous solution. Artif Organs. 1997 Jan;21(1):39-42.
26 Satta J, Lahtinen J, Raisanen L, Salmela E, Juvonen T. Options for the management of poststernotomy mediastinitis. Scand Cardiovasc J. 1998;32(1):29-32.
27 Ennker IC, Pietrowski D, Vohringer L, Kojcici B, Albert A, Vogt PM, et al. Surgical debridement, vacuum therapy and pectoralis plasty in poststernotomy mediastinitis. J Plast Reconstr Aesthet Surg. 2009 Nov;62(11):1479-1483.
28 Kadohama T, Akasaka N, Nagamine A, Nakanishi K, Kiyokawa K, Goh K, et al. Vacuum-assisted closure for pediatric post-sternotomy mediastinitis: are low negative pressures sufficient? Ann Thorac Surg. 2008 Mar;85(3):1094-1096.
29 Nesher N, Zlotnick AY, Porat E, Barak A, Bar-el Y, Uretzky G, et al. Right ventricular rupture following postoperative mediastinitis: a call for caution. Isr Med Assoc J. 2000 Sep;2(9):716-718.
30 Suen HC, Barner HB. Repair of right ventricular rupture complicating mediastinitis. Ann Thorac Surg. 1998 Dec;66(6):2115-2116.
31 Yellin A, Refaely Y, Paley M, Simansky D. Major bleeding complicating deep sternal infection after cardiac surgery. J Thorac Cardiovasc Surg. 2003 Mar;125(3):554-558.
32 Pairolero PC, Arnold PG. Management of recalcitrant median sternotomy wounds. J Thorac Cardiovasc Surg. 1984;88:357-364.
33 Schroeyers P, Wellens F, Degrieck I, De Geest R, Van Praet F, Vermeulen Y, et al. Aggressive primary treatment for poststernotomy acute mediastinitis: our experience with omental- and muscle flaps surgery. Eur J Cardiothorac Surg. 2001 Oct;20(4):743-746.
34 Ghazi BH, Carlson GW, Losken A. Use of the greater omentum for reconstruction of infected sternotomy wounds: a prognostic indicator. Ann Plast Surg. 2008 Feb;60(2):169-173.
35 Kaneda T, Aoshima M, Ishigami N, Iemura J, Matsumoto T. Successful treatment of MRSA mediastinitis after aortic arch replacement. Ann Thorac Cardiovasc Surg. 2000 Dec;6(6):414-417.
36 Shackcloth MJ, Edwards J, Griffiths EM. Management of sternal wound complications by high-pressure suction drainage via a polyurethane foam. Ann Thorac Surg. 2001 Sep;72(3):984.
37 Malmsjo M, Ingemansson R, Sjogren J. Mechanisms governing the effects of vacuum-assisted closure in cardiac surgery. Plast Reconstr Surg. 2007 Oct;120(5):1266-1275.
38 Lepelletier D, Poupelin L, Corvec S, Bourigault C, Bizouarn P, Blanloeil Y, et al. Risk factors for mortality in patients with mediastinitis after cardiac surgery. Arch Cardiovasc Dis. 2009 Feb;102(2):119-125.
39 Braxton JH, Marrin CA, McGrath PD, Morton JR, Norotsky M, Charlesworth DC, et al. 10-year follow-up of patients with and without mediastinitis. Semin Thorac Cardiovasc Surg. 2004;16(1):70-76.
40 Chang CH, Huang JY, Lai PC, Yang CW. Posterior mediastinal abscess in a hemodialysis patient—a rare but life-threatening complication of Staphylococcus bacteremia. Clin Nephrol. 2009 Jan;71(1):92-95.
41 Aerts JG, Kloover J, Los J, van der Heijden O, Janssens A, Tournoy KG. EUS-FNA of enlarged necrotic lymph nodes may cause infectious mediastinitis. J Thorac Oncol. 2008 Oct;3(10):1191-1193.
42 Katsetos MC, Tagbo AC, Lindberg MP, Rosson RS. Esophageal perforation and mediastinitis from fish bone ingestion. South Med J. 2003 May;96(5):516-520.
43 Blackmon SH, Correa AM, Wynn B, Hofstetter WL, Martin LW, Mehran RJ, et al. Propensity-matched analysis of three techniques for intrathoracic esophagogastric anastomosis. Ann Thorac Surg. 2007;83:1805-1813.
44 Studer SM, Heitmiller RF, Terry PB. Mediastinal abscess due to passage of a broncholith. Chest. 2002 Jan;121(1):296-297.
45 Fritscher-Ravens A, Schirrow L, Pothmann W, Knofel WT, Swain P, Soehendra N. Critical care transesophageal endosonography and guided fine-needle aspiration for diagnosis and management of posterior mediastinitis. Crit Care Med. 2003 Jan;31(1):126-132.
46 Bufkin BL, Miller JI, Mansour KA. Esophageal perforation: emphasis on management. Ann Thorac Surg. 1996;61:1447-1451.
47 Demirbag S, Tiryaki T, Atabek C, Surer I, Ozturk H, Cetinkursun S. Conservative approach to the mediastinitis in childhood secondary to esophageal perforation. Clin Pediatr. 2005 Mar;44(2):131-134.
48 Abbas G, Schuchert MJ, Pettiford BL, Pennathur A, Landreneau JL, et al. Contemporaneous management of esophageal perforation. Surgery. 2009 Oct;146(4):749-755.
49 Kotzampassakis N, Christodoulou M, Krueger T, Demartines N, Vuillemier H, Cheng C, et al. Esophageal leaks repaired by a muscle onlay approach in the presence of mediastinal sepsis. Ann Thorac Surg. 2009 Sep;88(3):966-972.
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